Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electrocardiograms of 90 patients with arteriographically documented acute submassive or massive pulmonary embolism and no associated cardiac or pulmonary disease were studied. Patients were derived from the Urokinase-Pulmonary Embolism Trial National Cooperative Study. In massive embolism, the electrocardiogram was normal in 6 per cent (3 of 50) of patients. With submassive embolism, 23 per cent of patients (9 of 40) had a normal electrocardiogram. Since one or more of the traditional manifestations of acute cor pulmonale (S1Q3T3, right bundle branch block, P pulmonale, or right axis deviation) occurred in only 26 per cent of patients, one could not rely exclusively upon these electrocardiographic abnormalities for the diagnosis of pulmonary embolism. The most common electrocardiographic abnormalities were nonspecific T wave changes which occurred in 42 per cent of patients and nonspecific abnormalities (elevation or depression) of the RST segment which occurred in 41 per cent of patients. Left axis deviation occurring in 7 per cent of the patients was as frequent as right axis deviation. Low voltage QRS complexes, previously undescribed in pulmonary embolism, occurred in 6 per cent of patients. None of the patients had atrial flutter or atrial fibrillation, which appears to occur more typically in patients with pulmonary embolism who have preexistent cardiac disease. All of the varieties of electrocardiographic abnormalities disappeared in some of the patients by 2 wk. Inversion of the T wave was the most persistent abnormality. Larger defects on the lung scan or pulmonary arteriogram occurred in patients with various abnormalities on the electrocardiogram than in patients with normal electrocardiograms. The pulmonary arterial mean pressure and/or right ventricular end-diastolic pressure was significantly higher in patients with several varieties of abnormal electrocardiograms, although the partial pressure of oxygen in arterial blood, in general, did not differ from that in patients with normal electrocardiograms. These hemodynamic correlations, made for the first time in patients, suggest that acute ventricular dilatation, possibly in combination with hypoxemia, is a causative factor of the electrocardiographic changes in acute massive or submassive pulmonary embolism.
Prog Cardiovasc Dis
PMID:The electrocardiogram in acute pulmonary embolism. 12 74

Maximal changes in haemodynamics and segmental wall motion were seen 2 min after coronary occlusion and were examined in relation to the loading conditions of the left ventricle before occlusion in 20 open chest dogs. There was a significant inverse relationship between the preligation mean aortic pressure and the percentage decrease in stroke volume following ligation. This relationship was observed whether afterload was distributed randomly (mean aortic pressure ranging from 9.7 to 17.6 kPa [73 to 132 mmHg]) between all dogs (r = 0.65; P less than 0.001) or altered by methoxamine (+4 kPa [+30 mmHg]) and nitroprusside (-3.2 kPa [-24 mmHg]) within the same dog (r = 0.82; P less than 0.001; n = 8). Although occlusion of the anterior descending artery caused a small (+5.5%) but significant increase in end-diastolic length of the non-ischaemic epicardial segment, the capacity for compensatory ventricular dilatation was not dependent on preligation afterload. However, the capacity of the ischaemic segment to undergo systolic expansion was significantly greater (+30.2% of end-systolic segment length) in those dogs with the lowest preligation MAP (8 to 12 kPa [60 to 90 mmHg]) compared with systolic lengthening of only 15.8% in the high afterload group (15 to 18 kPa [112 to 135 mmHg]). These data indicate that the loading conditions of the left ventricle predetermine the extent of global and segmental left ventricular dysfunction during the early phase of acute ischaemic injury.
Cardiovasc Res 1979 Mar
PMID:Afterload as a predeterminant of haemodynamics and segmental wall motion following coronary artery occlusion. 47 39

The pharmacologic treatment of atrial fibrillation (AF) is aimed at controlling the ventricular response, restoring sinus rhythm, and preventing or delaying relapses. In the control of ventricular response, digitalis maintains a primary role when the arrhythmia is accompanied by heart failure. In ischemic, hypertensive, and degenerative (whose number is increasing at present) cardiopathies without evident ventricular dilatation, treatments with calcium antagonists (such as verapamil, gallopamil, or diltiazem) or beta-blocking agents must be preferred. In order to control the ventricular response in patients with chronic AF during physical activity, the association of digitalis with beta-blocking agents or calcium antagonists seems to provide satisfactory results. The drugs of the IC class, especially flecainide, represent a certain therapeutical progress in the restoration of sinus rhythm in the treatment of paroxysmal atrial fibrillation affecting subjects without evident alterations of ventricular function, particularly in subjects with Wolff-Parkinson-White syndrome, with forms of vagal origin, or with atrial fibrillation alone. A therapeutic combination of digitalis and quinidine may produce resolution of the arrhythmia in the presence of altered ventricular function or when AF is of an uncertain onset. In patients with hypertensive, ischemic, and/or degenerative cardiopathy without evident ventricular or advanced heart failure, the verapamil-quinidine association may also be effective and even quicker. The combination of drugs of the I and III class for restoration of the sinus rhythm in particularly resistant forms of AF without evident structural heart alterations is promising but must be verified in a greater number of patients. In the prevention of relapses amiodarone appears to have the widest spectrum of advantages from an electrophysiologic point of view; however, because of its many side effects, amiodarone represents a late therapeutical choice. The promising results obtained with flecainide are disputed by the results of the CAST, which limit the possibilities of using this drug to a low number of cases (W.P.W. syndrome, AF of vagal origin, atrial fibrillation alone). In the past, quinidine and disopyramide have been the drugs most widely used in the prophylaxis of AF. These drugs have a similar efficacy, and both of them provided some positive results. However, because of untoward side effects (especially for quinidine) during chronic treatment, the use of these drugs has been questioned. Perhaps in the majority of patients, the less dangerous therapeutic choice after the termination of the fibrillation is a combination of drugs slowly down AV node activity (digitalis or calcium antagonists and beta blockers) with class IA antiarrhythmics.
Cardiovasc Drugs Ther 1991 Jun
PMID:The pharmacologic treatment of atrial fibrillation. 167 64

Of 1988 patients who underwent open-heart surgery from 1980 through 1988, 68 (3.4%) developed postoperative acute renal failure requiring dialysis (2.5% of adult and 8.3% of pediatric patients). Isolated aortocoronary bypass grafting was the operation with lowest incidence of this complication (0.6%). Acute renal failure usually appeared during the first 3 postoperative days. It carried a mortality rate of 63%, with half of the deaths occurring during the first few postoperative days, due to low cardiac output and progressive multiple organ failure. Logistic regression analysis in cases of aortic valve replacement demonstrated that significant independent preoperative risk factors for acute renal failure were renal insufficiency (serum creatinine greater than 110 mumol/l in greater than or equal to 2 samples) and increased cardiothoracic index/left ventricular end-diastolic dimension. Data from the literature indicated no time-related trend towards reduction of acute renal failure incidence or mortality. Prevention of low cardiac output is of major importance in these respects. Operative intervention before development of advanced disease with left ventricular dilatation and secondary kidney failure is advocated.
Scand J Thorac Cardiovasc Surg 1991
PMID:Prognosis and risk factors in acute, dialysis-requiring renal failure after open-heart surgery. 178 Jul 30

Hypertensive cardiac disease shows early alteration of left ventricular diastolic filling, characterized by a longer isovolumetric relaxation period and by an altered E/A ratio on the mitral spectral Doppler. We chose ten hypertensive patients who had left ventricular hypertrophy, but no left ventricular dilatation or mitral valve insufficiency and had a good left ventricular shortening fraction (greater than 26%). After the washout period we studied each of the above-mentioned parameters before and after the acute administration of nifedipine, dinitrate isosorbide, and captopril. While captopril and dinitrate isosorbide induced a prolongation of the isovolumic relaxation time and an impairment of the E/A ratio in mitral spectral Doppler (i.e., left ventricular filling), nifedipine induced an improvement in both parameters. The three drugs also induced a similar reduction in systemic blood pressure values (i.e., similar afterload). We therefore suggest that changes in diastolic function in hypertrophied cardiac fibers, induced by nifedipine, may be the result of a double action: one mediated by hemodynamic changes, the other directly affecting the cellular calcium ion exchange.
Cardiovasc Drugs Ther 1990 Aug
PMID:Effects of nifedipine on left ventricular diastolic function in hypertension; echo Doppler study. 207 6

An important antecedent to the development of late congestive heart failure is left ventricular dilatation and remodeling following myocardial infarction, which occurs in 30-40% of acute anterior transmural infarcts. Dilatation and remodeling commence within the first 24 hours following myocardial infarction and may be steadily progressive over months to years. Both the infarcted and uninfarcted regions of the myocardium are equally involved in the process. The remodeling process comprises left ventricular wall thinning (mainly due to cell slippage), chamber dilatation, and compensatory hypertrophy of the uninfarcted segment of the myocardium. The hypertrophy may initially be physiologic but may ultimately become a pathologic process, and thereby contribute to pump dysfunction. The possible reasons why the ventricular hypertrophy may ultimately be dysfunctional include alterations in local architecture and their sequelae alone or in concert with local changes in the beta-adrenergic, alpha-adrenergic, or renin angiotensin systems. At the present time, there are encouraging data to suggest that nitroglycerin, or the angiotensin converting enzyme inhibitor captopril, may ameliorate this process.
Cardiovasc Drugs Ther 1990 Oct
PMID:Left ventricular dilatation and failure post-myocardial infarction: pathophysiology and possible pharmacologic interventions. 214 59

Myocardial hypertrophy may influence coronary hemodynamics variably. Therefore, coronary blood flow (CBF) (gas chromatic argon technique) was determined in patients with left ventricular (LV) hypertrophy, with or without dilatation, associated with exclusively normal coronary arteriogram: 12 patients with hypertrophic obstructive cardiomyopathy (HOC) (LV mass to volume (M/V) ratio: 3.66 + 0.52 g/ml), 22 patients with hypertensive heart disease due to essential hypertension (EH) (LV M/V ratio: 2.12 + 0.26 g/ml), 18 patients with hypertensive dilatation (M/V ratio: 1.6 + 0.48 g/ml), 6 patients with aortic stenosis (LV M/V ratio: 1.99 + 0.41 g/ml), 12 patients with aortic incompetence (AI), 20 patients with normal heart function. CBF was determined as (A) controls and (B) following the intravenous injection of dipyridamole (0.5 mg/kg body weight). Coronary reserve (CR) was calculated as the ratio of coronary resistance before and after dipyridamole. Normal CR averaged 4.89 + 0.11 similar values despite marked LV hypertrophy, were present for both HOC (4.4 + 0.19) and as (4.66 + 0.12), whereas CR was considerably reduced in the concentrically hypertrophied hypertensive hearts (3.22 + 0.19) (p less than 0.001). Moderate decrease of CR was found in AI and in dilated EH. The results indicate that nonhypertensive hypertrophy, despite LV mass augmentation, may have normal CR, whereas at a comparable degree of LV hypertrophy, hypertensive hypertrophy has specific reduction in CR. Independent from vascular effects, ventricular dilatation may deteriorate CR because of an abnormal component of coronary vascular resistance.
J Cardiovasc Pharmacol 1985
PMID:Coronary hemodynamics in hypertensive heart disease: basic concepts and clinical consequences. 240 73

Beta-adrenoceptor antagonists do not directly depress myocardial contractile function. The primary pharmacological target of these drugs is to attenuate the increase in myocardial oxygen consumption resulting from sympathoadrenal stimulation of the heart. Pure beta blockade achieves this by modulating the increases in heart rate and myocardial contractility. This brings in its train the unwanted secondary and tertiary consequences of ventricular dilatation, impaired cardiac output response to exercise, and reflex increases in systemic vascular resistance and left ventricular afterload. Together these physiological effects offset much of the primary therapeutic benefit of these drugs. The ancillary pharmacological properties possessed by newer generations of beta-adrenoceptor antagonists have reduced some of the undesirable hemodynamic consequences of pure beta blockade. In this respect, positive inotropic activity and vasodilator effects, however achieved, are desirable properties in a drug with beta-blocking activity. Such additional pharmacodynamic activities afford direct support of cardiac contractile activity and reduce the undesirable increase in peripheral vasoconstriction that results from beta blockade alone. Celiprolol is a new dimension in beta-blocking therapy in that it achieves these additional hemodynamic benefits by widespread modulation of sympathoadrenal activity.
J Cardiovasc Pharmacol 1986
PMID:Beta-blocking drugs and myocardial function. 242 56

The hemodynamic and hormonal changes produced by adriamycin-induced cardiomyopathic congestive heart failure in rabbits were studied. Adriamycin cardiomyopathy in rabbits led to ventricular dilatation, pleural and pericardial effusions, hepatic congestion, and ascites. These pathological changes were associated with the maintenance of a normal blood pressure but a lowered cardiac output and increased total peripheral resistance. Plasma renin activity and plasma norepinephrine were increased twofold in rabbits with congestive cardiac failure. However, plasma vasopressin and osmolality were normal, whereas an increased vascular sensitivity to the infusion of exogenous vasopressin was demonstrated. Despite the normal levels of plasma vasopressin, administration of a specific vascular vasopressin antagonist led to a fall in blood pressure, a significant increase in cardiac output, and a decrease in total peripheral resistance. No such hemodynamic changes occurred on infusing normal rabbits with the vascular vasopressin antagonist, nor did any significant hemodynamic changes occur on injecting vehicle in rabbits with heart failure. These results suggest that in adriamycin-induced cardiomyopathic heart failure in rabbits, there is activation of the renin-angiotensin system and the sympathetic nervous system together with an increased sensitivity to vasopressin. These three hormonal systems help to maintain blood pressure by increasing total peripheral resistance in this experimental model of heart failure.
J Cardiovasc Pharmacol 1986
PMID:Role of vasopressin in experimental congestive cardiac failure. 243 82

Impairment of left ventricular function is a major consequence of acute myocardial infarction. Several interventions have been proposed to reduce the extent of myocardial tissue undergoing necrosis after cornoracy artery occlusion. Therapy for patients with acute myocardial infarction has long relied on interventions aimed at reducing oxygen consumption, such as administration of beta-blockers and nitrates. However, despite clinical evidence that these interventions can reduce mortality or prevent left ventricular dilatation, no clear benefit has been observed on left ventricular function. Over the past few years, treatment of acute myocardial infarction has radically changed. Availability of several thrombolytic agents has made reperfusion of ischemic myocardium a routine procedure. Early reperfusion has been shown to be the most powerful intervention to reduce infarct size and minimize left ventricular dysfunction in experimental preparations. Several clinical trials have also demonstrated that patients with acute myocardial infarction may greatly benefit from early thrombolysis, as this procedure is associated with improvement of global and regional left ventricular function and reduction in mortality. However, in spite of its obvious advantages, reperfusion might result in a paradoxical tissue damage that may blunt the net beneficial effect of restoring perfusion of ischemic myocardium. Reperfusion-mediated myocardial injury has been shown to occur in several experimental preparations and it has been proposed that generation of toxic oxygen metabolites at the moment of reflow is responsible for the occurrence of this phenomenon. Indeed, administration of free radical scavengers may significantly reduce the extent of reperfusion injury and improve contractile recovery in experimental preparations.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1989
PMID:Effects of pharmacological treatment of acute myocardial infarction on left ventricular function. 248 34


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